Funds were provided to us beginning June 1, 1983, to strengthen and expand our clinical research efforts in periodontal research. Using these funds, we expanded our studies of families manifesting an unusually high prevalence of early onset periodontitis, with the aim of clarifying the genetic aspects of these diseases as well as analyzing the pocket flora and correlating this with the pattern of serum antibodies reacting with putative periodontal pathogens. Pocket flora was sampled and cultured. Forty cultures were randomly selected and speciated. In collaboration with others, levels of serum antibodies reacting with any of a panel of 22 periodontal bacteria were measured using the ELISA technique. Similar studies were performed on a group of young children having the prepubertal form of peridontitis. We detected species of Fusobacterium, Selenomonas, Wolinella, Bacteroides and Capnocytophaga in the microflora of children with prepubertal periodontitis. In all except one case, onr or more of these species comprised a relatively large portion of the total isolates. With but one exception we failed to find Actinobacillus actinomycetemcomitans, Hemophilus aphrophilus and Bacteroides gingivalis. Serum antibodies reacting with one or more of the putative peridontal pathogens were found in eight of nine patients and included in order of prevalence C. sputigena, E. corrodens, B. intermedius, B. melaninogenicus, H. aphrophilus, and A. actinomycetemcomitans. In only one case did we find the microbial species in the subgingival microflora for which the patient had significant levels of antibodies in the serum. Furthermore, in all patients but one, we found relatively high portions of one or more species of Fusobacterium, Wolinella, Selenomonas, Bacteroides and Capnocytophaga in the subgingival flora but no antibodies reacting with these species in the serum. Studies on three families with a high prevalence of early onset peridontitis were completed and have been submitted for publication. The pattern and distribution of periodontitis in these families was consistent with that expected for an X-linked dominant genetic trait and inconsistent with an autosomal recessive trait as suggested by others.